Endotoxin-induced uveitis in rats and rabbits has served as a prototypical model to understand acute onset, intraocular inflammation. We now propose to clarify the pathogenesis of this model further by: 1) using immunohistology, in situ hybridization, immunoassay, bioassay or specific inhibitors to clarify the role of interleukin-1 and tumor necrosis factor in this inflammation; 2) use immunohistology or specific inhibitors of adhesion molecules to elucidate their role in this model; 3) determine the potential contribution of prostaglandin El to the antiinflammatory effects of endotoxin; 4) explore the role of gamma interferon in contributing to endotoxin induced eye effects; 5) determine if leumedins or soluble complement receptors are effective ocular anti-inflammatory agents. Collectively these studies should improve the understanding of the pathogenesis of endotoxin-induced uveitis. In addition, the experiments will determine the efficacy of novel modes of therapy for the inhibition of inflammation.